Evidence map›Paper›PMID 3680522›Full record

ArticleThe Journal of clinical investigation1987

Suppression of apolipoprotein B production during treatment of cholesteryl ester storage disease with lovastatin. Implications for regulation of apolipoprotein B synthesis.

H N Ginsberg, N A Le, M P Short, R Ramakrishnan, R J Desnick

Open access · bronzeAbstract readCase Reports
In one paragraph

Article in The Journal of clinical investigation, 1987. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 202 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  5. Review
  6. Article
  7. Review
  8. Article
  9. Statins and Cardiomyocyte Metabolism, Friend or Foe?Journal of cardiovascular development and disease · 2023
    Review
  10. Review
  11. Recent insights into lysosomal acid lipase deficiency.Trends in molecular medicine · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Influence ofFrontiers in pharmacology · 2018
    Article
  16. Review
  17. Article
  18. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 3 countries.

H N GinsbergDepartment of Medicine, Columbia University College of Physicians and Surgeons, Mount Sinai School of Medicine, New York, New York 10032.
N A Le
M P Short
R Ramakrishnan
R J Desnick
Columbia University · USIcahn School of Medicine at Mount Sinai · US

Funding

FABRY DISEASE: MOLECULAR AND MODEL THERAPEUTIC STUDIESR01AM034045 · AM · MOUNT SINAI SCHOOL OF MEDICINE OF CUNY · PI DESNICK, ROBERT J · 1985 to 1985
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REGULATION OF APOPROTEIN-B METABOLISM IN HUMANSR01HL036000 · NHLBI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI GINSBERG, HENRY N · 1985 to 1995
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NHLBI NIH HHS HL-23077NHLBI NIH HHS HL-36000NIADDK NIH HHS AM-34045
6 · The paper itself

Abstract

Cholesteryl ester storage disease (CESD) is characterized by the deficient activity of lysosomal cholesteryl ester (CE) hydrolase, accumulation of LDL-derived CE in lysosomes, and hyperlipidemia. We studied the kinetics of VLDL and LDL apolipoprotein B (apoB), using 125I-VLDL and 131I-LDL, in a 9-yr-old female with CESD and elevated total cholesterol (TC) (271.0 +/- 4.4 mg/dl), triglyceride (TG) (150.0 +/- 7.8 mg/dl), and LDL cholesterol (184.7 +/- 3.4 mg/dl). These studies demonstrated a markedly elevated production rate (PR) of apoB, primarily in LDL, with normal fractional catabolism of apoB in VLDL and LDL. Urine mevalonate levels were elevated, indicative of increased synthesis of endogenous cholesterol. Treatment with lovastatin, a competitive inhibitor of hydroxymethylglutaryl coenzyme A reductase, resulted in significant reductions in TC (196.8 +/- 7.9 mg/dl), TG (100.8 +/- 20.6 mg/dl), and LDL cholesterol (102.0 +/- 10.9 mg/dl). Therapy reduced VLDL apoB PR (5.2 vs. 12.2 mg/kg per d pretreatment) and LDL apoB PR (12.7 vs. 24.2 mg/kg per d pretreatment). Urine mevalonate levels also decreased during therapy. These results indicate that, in CESD, the inability to release free cholesterol from lysosomal CE resulted in elevated synthesis of endogenous cholesterol and increased production of apoB-containing lipoproteins. Lovastatin reduced both the rate of cholesterol synthesis and the secretion of apoB-containing lipoproteins.

Indexed as

Apolipoproteins BChildCholesterol EstersFemaleHumansLipid Metabolism, Inborn ErrorsLipoproteins, LDLLipoproteins, VLDLLovastatinApolipoproteins BCholesterol EstersLipoproteins, LDLLipoproteins, VLDLLovastatin

Identifiers

PMID3680522
PMCPMC442441
OpenAlexW2104602624

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.